| 2000 |
KIF17 directly interacts with the PDZ domain of mLin-10 (Mint1/X11) via its tail domain, linking KIF17 to a large protein complex (mLin-2/CASK, mLin-7/MALS/Velis, NR2B) and enabling transport of NR2B-containing vesicles along microtubules in neuronal dendrites. |
Co-immunoprecipitation, direct interaction pulldown, in vitro microtubule transport assay |
Science |
High |
10846156
|
| 2003 |
KIF17 vesicles move processively along dendrites at ~0.76 μm/sec and are associated with extrasynaptic NR2B; knockdown or dominant-negative blockade of KIF17 significantly reduces NR2B expression and synaptic localization, with a compensatory increase in synaptic NR2A. |
Live-cell imaging in hippocampal neurons, dominant-negative expression, siRNA knockdown, immunostaining |
The Journal of Neuroscience |
High |
12514209
|
| 2002 |
Overexpression of KIF17 in transgenic mice upregulates NR2B expression with increased CREB phosphorylation, enhancing spatial and working memory, establishing KIF17 as an in vivo regulator of NR2B trafficking and synaptic plasticity. |
Transgenic mouse overexpression, behavioral tasks, Western blotting, immunohistochemistry |
PNAS |
High |
12391294
|
| 2007 |
CaMKII phosphorylates KIF17 at Ser1029 in its tail domain, disrupting the KIF17–Mint1 interaction and causing release of the NR2B cargo from microtubule-based transport, establishing a phosphorylation-dependent cargo release mechanism. |
FRET-based protein-protein interaction assay, in vitro kinase assay, site-directed mutagenesis, in vivo approaches |
Nature Cell Biology |
High |
18066053
|
| 2010 |
KIF17 contains a ciliary localization signal (CLS) in its tail domain homologous to nuclear localization signals (NLSs); ciliary entry of KIF17 is regulated by importin-β2 binding (dependent on CLS and inhibited by RanGTP) and a ciliary-cytoplasmic RanGTP gradient, analogous to nuclear import. |
Deletion/mutagenesis of CLS, co-immunoprecipitation with importin-β2, dominant-negative RanG19V expression, live-cell fluorescence imaging |
Nature Cell Biology |
High |
20526328
|
| 2006 |
KIF17 is required for ciliary targeting of olfactory CNG channels in mammalian olfactory sensory neurons; the CNGB1b subunit's RVxP motif is necessary for this KIF17-dependent transport into cilia. |
Dominant-negative KIF17 expression, immunofluorescence, subcellular fractionation in olfactory epithelium |
Current Biology |
High |
16782012
|
| 2008 |
In zebrafish photoreceptors, Kif17 co-localizes with IFT proteins within the outer segment (OS), co-immunoprecipitates with IFT proteins, and knockdown of Kif17 severely disrupts OS formation and visual pigment targeting, establishing Kif17 as essential for photoreceptor OS development via IFT. |
Co-immunoprecipitation, morpholino knockdown in zebrafish, immunofluorescence, electron microscopy |
Developmental Biology |
High |
18304522
|
| 2011 |
In kif17-/- mice, NR2B transport is inhibited and nr2b transcription is decreased; NR2A levels are also reduced through accelerated ubiquitin-proteasome-dependent degradation. NMDAR-mediated synaptic currents, LTP, LTD, and CREB responses are attenuated, causing hippocampus-dependent memory impairment. |
Kif17 knockout mouse, electrophysiology, behavioral tests, Western blotting, ubiquitin-proteasome pathway analysis |
Neuron |
High |
21521616
|
| 2012 |
Phosphorylation of KIF17 at Ser1029 (by CaMKII) controls both loading and unloading of GluN2B cargo in vivo; phosphomimetic (S1029D) and phospho-null (S1029A) transgenic mice in kif17-/- background both show reduced synaptic NMDA receptors, impaired plasticity, and spatial memory deficits due to inability to properly load/unload GluN2B. |
Transgenic phosphomutant mice in kif17-/- background, electrophysiology, behavioral tests, immunostaining |
The Journal of Neuroscience |
High |
22514311
|
| 2005 |
KIF17 transports the dendritic K+ channel Kv4.2 to dendrites; dominant-negative KIF17 inhibits Kv4.2 dendritic localization, Kv4.2 co-immunoprecipitates with KIF17 from brain lysate, and the interaction is mediated through the extreme C-terminus of Kv4.2. |
Dominant-negative expression, co-immunoprecipitation from brain and COS cells, immunofluorescence in cortical neurons |
The Journal of Biological Chemistry |
High |
16257958
|
| 2006 |
KIF17 interacts with kainate receptor subunits GluR6 and KA2, and is required for localization of GluR5-containing kainate receptors to distal dendrites of hippocampal neurons, establishing KIF17 as a motor for this receptor subtype. |
Co-immunoprecipitation, dominant-negative KIF17 expression, immunofluorescence in hippocampal neurons |
Molecular and Cellular Neurosciences |
Medium |
17174564
|
| 2006 |
The testis-specific KIF17b physically interacts with MIWI (a PIWI/Argonaute family member) in chromatoid bodies of round spermatids; KIF17b localizes in chromatoid bodies and its presence offers a mechanism for microtubule-dependent chromatoid body mobility and transport of RNA components. |
Co-immunoprecipitation, immunofluorescence, live imaging of chromatoid body movement |
Journal of Cell Science |
Medium |
16787948
|
| 2003 |
KIF17b co-immunoprecipitates with TB-RBP (Translin) in an RNA-protein complex containing specific CREM-regulated mRNAs; KIF17b functions as a motor component of an mRNP complex transporting CREM-regulated mRNAs in male postmeiotic germ cells, with TB-RBP release coinciding with the time of mRNA translation. |
Co-immunoprecipitation, in vivo RNA-protein crosslinking, in situ hybridization combined with immunohistochemistry at EM level, transfection assays |
PNAS |
Medium |
14673085
|
| 2005 |
KIF17b's nucleocytoplasmic shuttling and transport of the transcriptional coactivator ACT (activator of CREM in testis) are independent of its motor domain and microtubules; instead, protein kinase A phosphorylates KIF17b and regulates its subcellular localization. |
Motor domain deletion mutants, microtubule depolymerization assays, PKA inhibition, immunofluorescence |
The Journal of Biological Chemistry |
Medium |
16002395
|
| 2013 |
The KIF17 motor domain (K370) directly stabilizes microtubule plus-ends and inhibits depolymerization independently of EB1, while the KIF17 autoinhibitory tail domain binds MTs and tubulin dimers, delaying MT polymerization; EB1 and KIF17-Tail competitively modulate K370 ATPase activity. |
In vitro MT dynamic instability assays, in vitro ATPase assays, MT gliding assay, cell-based nocodazole depolymerization assay, domain truncation/competition experiments |
The Journal of Biological Chemistry |
High |
24072717
|
| 2016 |
KIF17 localizes at cell-cell adhesions and its motor domain (independent of microtubule binding) activates RhoA-GTPase signaling via RhoA→ROCK→LIMK→cofilin pathway to drive junctional actin remodeling and stabilize the apical junctional complex in epithelial cells. |
KIF17 KD and OE with truncation mutants, active RhoA pulldown assay, ROCK/LIMK inhibitors, actin incorporation assay, 3D organotypic cultures |
Journal of Cell Science |
Medium |
26759174
|
| 2016 |
Polarized dendritic targeting of KIF17 operates via three steps: (1) cargo binding relieves KIF17 autoinhibition and initiates transport; (2) KIF17-vesicles enter axons but are excluded by the actin cytoskeleton at the axon initial segment (AIS); (3) dynein activity redirects KIF17-coupled cargoes into dendrites. |
Live-cell imaging with inducible trafficking assays, actin depolymerization at AIS, dynein inhibition, dominant-negative constructs in neurons |
Current Biology |
High |
27265394
|
| 2016 |
Septin 9 (SEPT9) directly associates with the C-terminal tail of KIF17 (the cargo-binding domain), preferentially in the extended conformation, and competitively interferes with mLin-10/Mint1 PDZ1 binding to KIF17, thereby downregulating NR2B transport into dendrites without affecting KIF17 microtubule-dependent motility. |
Direct binding assay (in vitro), co-immunoprecipitation, live-cell imaging of KIF17 motility, NR2B transport assay in hippocampal neurons, domain mapping |
Molecular Biology of the Cell |
High |
26823018
|
| 2017 |
KIF17 interacts with the IFT46-IFT56 dimer of the IFT-B complex through its C-terminal sequence immediately upstream of the NLS; ciliary entry of KIF17 requires both IFT-B binding and its NLS (which binds importin-α), but KIF17 is dispensable for ciliogenesis and IFT-B intraciliary trafficking in mammalian cells. |
Visible immunoprecipitation (VIP) assay, deletion/truncation mutants, co-immunoprecipitation, fluorescence imaging |
Molecular Biology of the Cell |
High |
28077622
|
| 2015 |
D1-type dopamine receptors are delivered to the ciliary membrane from the extra-ciliary plasma membrane via a mechanism requiring IFT-B complex and KIF17; Rab23 (a small GTPase) is essential for this process, as Rab23 depletion prevents receptor ciliary access and Rab23 fusion to a non-ciliary receptor drives its ciliary targeting. |
siRNA depletion of IFT-B/KIF17/Rab23, receptor chimeras, fluorescence imaging, nucleotide-dependent Rab23 fusion constructs |
eLife |
High |
26182404
|
| 2015 |
Rab23 exists in a complex with KIF17 and importin-β2, and Rab23 depletion disrupts ciliary localization of KIF17; active Rab23 (Q68L) localizes to cilia and promotes KIF17 ciliary targeting through a mechanism distinct from Ran-GTP. |
Co-immunoprecipitation, affinity-binding studies, siRNA depletion, immunofluorescence, constitutively active/inactive Rab23 mutants |
Journal of Cell Science |
Medium |
26136363
|
| 2018 |
CaMKII-mediated phosphorylation of KIF17 at S815 (zebrafish)/S1029 (mouse) promotes its localization along the cone outer segment and drives photoreceptor outer segment disc shedding in a cell-autonomous manner; constitutively active tCaMKII increases disc shedding in a kif17-dependent manner. |
Transgenic zebrafish with phosphomimetic/phospho-null KIF17, genetic kif17 mutants, disc shedding assay, constitutively active CaMKII expression |
BMC Cell Biology |
High |
30458707
|
| 2019 |
GTP-bound Rab23 recruits Kif17 to meiotic spindle poles in mouse oocytes; Kif17 regulates tubulin acetylation by associating with αTAT and Sirt2, and its tail domain interacts with the RhoA-ROCK-LIMK-cofilin pathway to modulate actin filament assembly needed for spindle migration to the cortex during meiosis. |
siRNA depletion of Rab23/Kif17, co-immunoprecipitation of tail domain with pathway components, immunofluorescence, polar body extrusion assays in mouse oocytes |
Development |
Medium |
30696709
|
| 2020 |
KIF17 is locally degraded and synthesized in an NMDAR-mediated activity-dependent manner in individual dendrites; local KIF17 synthesis is driven by its 3'UTR, and hippocampus-specific deletion of Kif17 3'UTR impairs fear memory extinction by disrupting activity-dependent local KIF17 synthesis. |
NMDAR antagonist/agonist treatment, dendritic local synthesis assay, 3'UTR deletion mouse model, fear memory behavioral assays, fluorescence imaging |
Science Advances |
High |
33328231
|
| 2017 |
KIF17 interacts with the orphan nuclear receptor ERR1 (ERRα) via its C-terminal tail domain (through an LXXLL nuclear receptor box motif); KIF17 tail expression attenuates nuclear accumulation of ERR1 and inhibits its transcriptional activity, while KIF17 knockout elevates ERR1 activity. |
Yeast-2-hybrid screen, in vitro biochemical binding assay, domain mapping, ERR1 transcriptional reporter assay, KIF17 KO cells, nuclear localization imaging |
Oncotarget |
Medium |
28881568
|
| 2013 |
Mouse TTC30B (ortholog of C. elegans DYF-1) interacts with KIF17 and multiple IFT-B complex proteins, suggesting TTC30B links KIF17 to the IFT-B complex for ciliary transport. |
Co-immunoprecipitation from pituitary cells, mass spectrometry, cell-free co-immunoprecipitation |
Experimental Cell Research |
Medium |
23810713
|
| 2006 |
OSM-3 (C. elegans KIF17 ortholog) is autoinhibited in solution through an intramolecular interaction involving folding at a central hinge; a point mutation (G444E) in the hinge or hinge deletion activates ATPase activity and processive movement, and cargo attachment to beads also relieves autoinhibition. |
Single-molecule fluorescence motility assay, MT-stimulated ATPase assay, point mutations, optical trap, conformation analysis by electron microscopy |
The Journal of Cell Biology |
High |
17000874
|
| 2021 |
Crystal structures of the OSM-3 (KIF17 ortholog) motor domain in ADP-bound, nucleotide-free, and ATP-analog-bound states show that OSM-3 shares an identical nucleotide-binding site with kinesin-5 Eg5, supporting a universal two-water ATP hydrolysis mechanism in the kinesin superfamily including kinesin-2. |
X-ray crystallography of OSM-3 motor domain in multiple nucleotide states, structural comparison |
FEBS Open Bio |
High |
33513284
|
| 2024 |
KIF17 has dual opposing roles in HH-dependent cerebellar development: in Purkinje cells (HH-producing), KIF17 deletion reduces SHH protein levels and decreases CGNP proliferation; in CGNPs (HH-responding), KIF17 deletion increases HH target gene expression and CGNP proliferation through altered GLI transcription factor processing. |
Germline and cell-type-specific conditional Kif17 knockout mice, HH pathway target gene expression analysis, SHH protein quantification, cerebellar morphometry |
Science Advances |
High |
38669326
|
| 2022 |
KIF17 is modified by SUMOylation, which contributes to its stabilization and maintenance in epileptic neurons; KIF17 overexpression increases NR2B membrane expression and excitatory synaptic transmission, whereas knockdown has the opposite effect. |
Kainic acid epilepsy mouse model, KIF17 OE/KD, electrophysiology, SUMO modification assay, Western blotting |
Neuroscience Bulletin |
Medium |
35678994
|
| 2006 |
Spatial-ε protein co-localizes and co-immunoprecipitates with KIF17b in spermatid manchette and sperm tail principal piece, establishing Spatial-ε as a KIF17b cargo during spermatogenesis. |
Co-immunoprecipitation from testis lysates, indirect immunofluorescence co-localization |
Experimental Cell Research |
Medium |
17196196
|